Cardiovascular Toxicology

, Volume 2, Issue 3, pp 165–180

Oxidative stress promotes blood cell-endothelial cell interactions in the microcirculation

  • Dianne Cooper
  • Karen Y. Stokes
  • Anitaben Tailor
  • D. Neil Granger
Article

DOI: 10.1007/s12012-002-0002-7

Cite this article as:
Cooper, D., Stokes, K.Y., Tailor, A. et al. Cardiovasc Toxicol (2002) 2: 165. doi:10.1007/s12012-002-0002-7

Abstract

Oxidative stress occurs when the production of reactive oxygen species (ROS) exceeds the capacity of the cell to detoxify these potentially injurious oxidants using endogenous antioxidant defense systems. Conditions associated with oxidative stress include ischemia/reperfusion, hypercholesterolemia, diabetes, and hypertension. The adhesion of circulating blood cells (leukocytes, platelets) to vascular endothelium is a key element of the pro-inflammatory and prothrombogenic phenotype assumed by the vasculature in these and other disease states that are associated with an oxidative stress. There is a growing body of evidence that links the blood cell-endothelial cell interactions in these conditions to the enhanced production of ROS. Potential enzymatic sources of ROS within the microcirculation include xanthine oxidase, NAD(P)H oxidase, and nitric oxide synthase. ROS can promote a pro-inflammatory/prothrombogenic phenotype within the microvasculature by a variety of mechanisms, including the inactivation of nitric oxide, the activation of redox-sensitive transcription factors (e.g., nuclear factor-ξB) that govern the expression of endothelial cell adhesion molecules (e.g., P-selectin), and the activation of enzymes (e.g., phospholipase A2) that produce leukocyte-stimulating inflammatory mediators (e.g., platelet-activating factor). The extensively documented ability of different oxidant-ablating interventions to attenuate blood cell-endothelial cell interactions underscores the importance of ROS in mediating the dysfunctional microvascular responses to oxidative stress.

Key Words

Oxidative stresssuperoxideendothelial cellsnitric oxideleukocytes

Copyright information

© Humana Press Inc. 2002

Authors and Affiliations

  • Dianne Cooper
    • 1
  • Karen Y. Stokes
    • 1
  • Anitaben Tailor
    • 1
  • D. Neil Granger
    • 1
  1. 1.Department of Molecular and Cellular PhysiologyLouisiana State University Health Sciences CenterShreveport